Why the DHT cope should END ASAP.

[TheTD7]

Believe it or not, there are still retards on this site + IRL that genuinely believe DHT muh "masculinizes your face". It should be known by now that DHT is one of the most useless hormones when it comes to attractiveness post 16-18 years of age.
​

Table of Contents:
1. Molecular/Enzymatic basis
1.1. Synthesis and Potency.
1.2. Aromatization constraint.
1.3. Intracrine/paracrine compartmentalization.

2. Facial Bones
2.1. Ossification.
2.2. Androgens (more specifically androgenic morphogenesis).
2.3. Epiphyseal maturation.

3. Cellular Constraints
3.1. AR signaling
3.2. Estrogenic signaling (important)
3.3. Cofactor/Chromatin Context

4. Follicular Biology
4.1. Follicular miniaturization.
4.2. Skin Texture
4.3. Regional Specificity



1. Molecular/Enzymatic basis:
Synthesis and potency: Testosterone is converted to DHT by 5AR, basic knowledge (isoenzymes SRD5A1 and SRD5A2). DHT has around 5 x higher affinity for AR and forms a more stable AR-ligand complex, producing a MUCHHH stronger transcriptional activation at androgen response elements. This makes DHT the dominant androgenic effector in tissues with high 5AR activity (skin, hair follicle dermal papilla etc..). So now your retarded brain (doesn't apply to you if you're anti DHT) knows the basics of what we're facing.

Aromatization constraint: DHT is not a substrate for aromatase (CYP19A1) so basically it js means it cannot be converted into estradiol. AND GUESS FUCKING WHAT? ESTRADIOL IS a CENTRAL MEDIATOR of epiphyseal fusion & bone mineralization. Because DHT cannot even yield fucking estrogenic metabolites, so logically its ability to influence bone (via ER pathway) is...... NIL. NADA. ZERO.

Intracrine/paracrine compartmentalization: Androgen action is contextual, that is, local intracellular conversion and paracrine mediators (IGF1, TGF-beta (can't find symbol lol) family, Wnt/beta-catenin modulators) determine the phenotype. The scalp and facial dermis have a fuck ton of SRD5A expressions so DHT collects in soft tissues where it exerts trophic/atrophic effects depending on cell type. Bone cells express AR but their response is modulated by..... you guessed it, estrogen receptor signaling.


2. Facial Bones
Ossification: Facial bones arise mainly by direct differentiation of mesenchymal cells into osteoblasts (obv there are contributions from sutural growth + periosteal apposition). Maxillofacial size/shape are changed during puberty, obv, by a combo of endochondral growth at cranial base synchondroses + periosteal modeling. So the ossification part is clear, that's another step in understanding the final verdict (title, lol.).

Androgenic Morphogenesis: The ABSOLUTE most plastic period for changing ur face is ofc the pubertal window, when chondrocytes and osteoprogenitors are proliferative, sutures are patent and periosteal apposition rates are high. Androgens in this window help iin periosteal expansion (increasing bone breadth) by AR signaling in osteoblast lineage cells + androgen to estradiol conversion that influences endochondral maturation and death of growth plates (closure = death hehe).

Epiphyseal maturation: By 17-19 years *most* craniofacial growth centers undergo reduced chondrogenesis and sutural interdigitation increases and the proliferative capacity of osteoprogenitors gets fucked (diminishes). Once the osteogenic niche has transitioned from high turnover developmental modeling to low turnover remodeling, the capacity for ACTUAL, GOOD AMT. of periosteal expansion is pretty less/minimal/near zero or whatever. Basically by 17 you're nearing completion. This is basic knowledge but i wanted to provide a small amount of insight into the actual process.

3. Cellular Constraints
AR signaling: Osteoblasts, osteocytes nd mesenchymal progenitors express AR. DHT binding can change osteoblastic differentiation and local RANKL or OPG balance (not important to know, but if you wanna know js tell me). But a good amt. of periosteal expansion requires proliferation of osteoprogenitors which is variant and..... BOOM, age dependent. So you're done by late teens. Like 17-18-19 means it's literally 99% over.

Estrogenic signaling: A lotta anabolic skeletal effects are attributed to androgens are actually mediated by aromatization to estradiol and then, ER signaling. Because DHT bypasses aromatase (as we read in 1.2.), it lacks a HUGGEEE PART that drives bone geometry in adults.

Cofactor/Chromatin context: Whether DHT changes a cell’s behavior depends on what helper proteins and DNA regions are available for the AR to work with. In mature bone (what we're talking abt), the genes that control growth and shape are mostly fucked, and only maintenance genes stay active. Even though DHT binds the AR it can’t turn on the old growth. So even a high affinity ligand like DHT yields constrained outputs.


4. Follicular Biology
Follicular Miniaturization: AAAANNNDDDD WE HAVE REACHED THE MAIN PART. Androgenic alopecia is a classic DHT mediated phenotype. In genetically susceptible follicles (AR polymorphisms, CAG repeat length, local SRD5A expression), DHT-AR transcriptional activity upregulates paracrine mediators like TGF-beta1/2, DKK1 that induce miniaturization, which, if your retard brain doesn't understand, basically means progressive shortening of the anagen phase, reduction of the hair follicle’s dermal papilla signals and replacement of terminal hair shafts with vellus hair.

Skin Texture: DHT actuvates sebaceous gland lipogenesis by AR driven expression of enzymes of lipid biosynthesis, increasing sebum production and pore prominence. Now obviously who on the fucking planet would want that? Yup, members of the pro DHT clan. JFL at them.

Regional specificity: The same androgenic milieu can masculinize secondary sexual traits (laryngeal hypertrophy, facial hair) but in a weird way cause hair loss on the scalp. This is a dichotomy. And this dichotomy is due to region specific AR cofactor expression and differential paracrine signaling in the ffollicular units (No need to get into details as our main topic has been cleared already)



SO, I GUESS THAT'S ENOUGH TO SHUT DOWN DHT COPES? BUT, I SERIOUSLY DON'T UNDERSTAND WHY ANYONE WOULD NEED DHT POST 17. REALLY MAKES ME CURIOUS.

​

 

[LXR]

Kevin Mann I caught you lacking bud

 

[User28823]

there are cognitive and sexual benefits of dht

i take 5-ar inhibitors but even i recognize these

 

[IrishSlayer1483]

Believe it or not, there are still retards on this site + IRL that genuinely believe DHT muh "masculinizes your face". It should be known by now that DHT is one of the most useless hormones when it comes to attractiveness post 16-18 years of age.
​

Table of Contents:
1. Molecular/Enzymatic basis
1.1. Synthesis and Potency.
1.2. Aromatization constraint.
1.3. Intracrine/paracrine compartmentalization.

2. Facial Bones
2.1. Ossification.
2.2. Androgens (more specifically androgenic morphogenesis).
2.3. Epiphyseal maturation.

3. Cellular Constraints
3.1. AR signaling
3.2. Estrogenic signaling (important)
3.3. Cofactor/Chromatin Context

4. Follicular Biology
4.1. Follicular miniaturization.
4.2. Skin Texture
4.3. Regional Specificity



1. Molecular/Enzymatic basis:
Synthesis and potency: Testosterone is converted to DHT by 5AR, basic knowledge (isoenzymes SRD5A1 and SRD5A2). DHT has around 5 x higher affinity for AR and forms a more stable AR-ligand complex, producing a MUCHHH stronger transcriptional activation at androgen response elements. This makes DHT the dominant androgenic effector in tissues with high 5AR activity (skin, hair follicle dermal papilla etc..). So now your retarded brain (doesn't apply to you if you're anti DHT) knows the basics of what we're facing.

Aromatization constraint: DHT is not a substrate for aromatase (CYP19A1) so basically it js means it cannot be converted into estradiol. AND GUESS FUCKING WHAT? ESTRADIOL IS a CENTRAL MEDIATOR of epiphyseal fusion & bone mineralization. Because DHT cannot even yield fucking estrogenic metabolites, so logically its ability to influence bone (via ER pathway) is...... NIL. NADA. ZERO.

Intracrine/paracrine compartmentalization: Androgen action is contextual, that is, local intracellular conversion and paracrine mediators (IGF1, TGF-beta (can't find symbol lol) family, Wnt/beta-catenin modulators) determine the phenotype. The scalp and facial dermis have a fuck ton of SRD5A expressions so DHT collects in soft tissues where it exerts trophic/atrophic effects depending on cell type. Bone cells express AR but their response is modulated by..... you guessed it, estrogen receptor signaling.


2. Facial Bones
Ossification: Facial bones arise mainly by direct differentiation of mesenchymal cells into osteoblasts (obv there are contributions from sutural growth + periosteal apposition). Maxillofacial size/shape are changed during puberty, obv, by a combo of endochondral growth at cranial base synchondroses + periosteal modeling. So the ossification part is clear, that's another step in understanding the final verdict (title, lol.).

Androgenic Morphogenesis: The ABSOLUTE most plastic period for changing ur face is ofc the pubertal window, when chondrocytes and osteoprogenitors are proliferative, sutures are patent and periosteal apposition rates are high. Androgens in this window help iin periosteal expansion (increasing bone breadth) by AR signaling in osteoblast lineage cells + androgen to estradiol conversion that influences endochondral maturation and death of growth plates (closure = death hehe).

Epiphyseal maturation: By 17-19 years *most* craniofacial growth centers undergo reduced chondrogenesis and sutural interdigitation increases and the proliferative capacity of osteoprogenitors gets fucked (diminishes). Once the osteogenic niche has transitioned from high turnover developmental modeling to low turnover remodeling, the capacity for ACTUAL, GOOD AMT. of periosteal expansion is pretty less/minimal/near zero or whatever. Basically by 17 you're nearing completion. This is basic knowledge but i wanted to provide a small amount of insight into the actual process.

3. Cellular Constraints
AR signaling: Osteoblasts, osteocytes nd mesenchymal progenitors express AR. DHT binding can change osteoblastic differentiation and local RANKL or OPG balance (not important to know, but if you wanna know js tell me). But a good amt. of periosteal expansion requires proliferation of osteoprogenitors which is variant and..... BOOM, age dependent. So you're done by late teens. Like 17-18-19 means it's literally 99% over.

Estrogenic signaling: A lotta anabolic skeletal effects are attributed to androgens are actually mediated by aromatization to estradiol and then, ER signaling. Because DHT bypasses aromatase (as we read in 1.2.), it lacks a HUGGEEE PART that drives bone geometry in adults.

Cofactor/Chromatin context: Whether DHT changes a cell’s behavior depends on what helper proteins and DNA regions are available for the AR to work with. In mature bone (what we're talking abt), the genes that control growth and shape are mostly fucked, and only maintenance genes stay active. Even though DHT binds the AR it can’t turn on the old growth. So even a high affinity ligand like DHT yields constrained outputs.


4. Follicular Biology
Follicular Miniaturization: AAAANNNDDDD WE HAVE REACHED THE MAIN PART. Androgenic alopecia is a classic DHT mediated phenotype. In genetically susceptible follicles (AR polymorphisms, CAG repeat length, local SRD5A expression), DHT-AR transcriptional activity upregulates paracrine mediators like TGF-beta1/2, DKK1 that induce miniaturization, which, if your retard brain doesn't understand, basically means progressive shortening of the anagen phase, reduction of the hair follicle’s dermal papilla signals and replacement of terminal hair shafts with vellus hair.

Skin Texture: DHT actuvates sebaceous gland lipogenesis by AR driven expression of enzymes of lipid biosynthesis, increasing sebum production and pore prominence. Now obviously who on the fucking planet would want that? Yup, members of the pro DHT clan. JFL at them.

Regional specificity: The same androgenic milieu can masculinize secondary sexual traits (laryngeal hypertrophy, facial hair) but in a weird way cause hair loss on the scalp. This is a dichotomy. And this dichotomy is due to region specific AR cofactor expression and differential paracrine signaling in the ffollicular units (No need to get into details as our main topic has been cleared already)



SO, I GUESS THAT'S ENOUGH TO SHUT DOWN DHT COPES? BUT, I SERIOUSLY DON'T UNDERSTAND WHY ANYONE WOULD NEED DHT POST 17. REALLY MAKES ME CURIOUS.

​

if you have no balding genes you shouldnt use fin or dut just for slight frame improvements you can get, i agree dht doesnt masculinise faces thats genes

 

[m0ss26]

there are cognitive and sexual benefits of dht

i take 5-ar inhibitors but even i recognize these

It depends though, some people have no difference in cognition or sexual function even with their DHT shot

 

[m0ss26]

Good thread

DHT = trash

 

[TheTD7]

bump

 

[BrickTop]

Recently used Andractim (DHT Gel), sexual endurance/orgasm was 1000x better than before.

Yes, DHT is useless if you don't plan on having sex with women post 16-18.

 

[unkownincel]

Believe it or not, there are still retards on this site + IRL that genuinely believe DHT muh "masculinizes your face". It should be known by now that DHT is one of the most useless hormones when it comes to attractiveness post 16-18 years of age.
​

Table of Contents:
1. Molecular/Enzymatic basis
1.1. Synthesis and Potency.
1.2. Aromatization constraint.
1.3. Intracrine/paracrine compartmentalization.

2. Facial Bones
2.1. Ossification.
2.2. Androgens (more specifically androgenic morphogenesis).
2.3. Epiphyseal maturation.

3. Cellular Constraints
3.1. AR signaling
3.2. Estrogenic signaling (important)
3.3. Cofactor/Chromatin Context

4. Follicular Biology
4.1. Follicular miniaturization.
4.2. Skin Texture
4.3. Regional Specificity



1. Molecular/Enzymatic basis:
Synthesis and potency: Testosterone is converted to DHT by 5AR, basic knowledge (isoenzymes SRD5A1 and SRD5A2). DHT has around 5 x higher affinity for AR and forms a more stable AR-ligand complex, producing a MUCHHH stronger transcriptional activation at androgen response elements. This makes DHT the dominant androgenic effector in tissues with high 5AR activity (skin, hair follicle dermal papilla etc..). So now your retarded brain (doesn't apply to you if you're anti DHT) knows the basics of what we're facing.

Aromatization constraint: DHT is not a substrate for aromatase (CYP19A1) so basically it js means it cannot be converted into estradiol. AND GUESS FUCKING WHAT? ESTRADIOL IS a CENTRAL MEDIATOR of epiphyseal fusion & bone mineralization. Because DHT cannot even yield fucking estrogenic metabolites, so logically its ability to influence bone (via ER pathway) is...... NIL. NADA. ZERO.

Intracrine/paracrine compartmentalization: Androgen action is contextual, that is, local intracellular conversion and paracrine mediators (IGF1, TGF-beta (can't find symbol lol) family, Wnt/beta-catenin modulators) determine the phenotype. The scalp and facial dermis have a fuck ton of SRD5A expressions so DHT collects in soft tissues where it exerts trophic/atrophic effects depending on cell type. Bone cells express AR but their response is modulated by..... you guessed it, estrogen receptor signaling.


2. Facial Bones
Ossification: Facial bones arise mainly by direct differentiation of mesenchymal cells into osteoblasts (obv there are contributions from sutural growth + periosteal apposition). Maxillofacial size/shape are changed during puberty, obv, by a combo of endochondral growth at cranial base synchondroses + periosteal modeling. So the ossification part is clear, that's another step in understanding the final verdict (title, lol.).

Androgenic Morphogenesis: The ABSOLUTE most plastic period for changing ur face is ofc the pubertal window, when chondrocytes and osteoprogenitors are proliferative, sutures are patent and periosteal apposition rates are high. Androgens in this window help iin periosteal expansion (increasing bone breadth) by AR signaling in osteoblast lineage cells + androgen to estradiol conversion that influences endochondral maturation and death of growth plates (closure = death hehe).

Epiphyseal maturation: By 17-19 years *most* craniofacial growth centers undergo reduced chondrogenesis and sutural interdigitation increases and the proliferative capacity of osteoprogenitors gets fucked (diminishes). Once the osteogenic niche has transitioned from high turnover developmental modeling to low turnover remodeling, the capacity for ACTUAL, GOOD AMT. of periosteal expansion is pretty less/minimal/near zero or whatever. Basically by 17 you're nearing completion. This is basic knowledge but i wanted to provide a small amount of insight into the actual process.

3. Cellular Constraints
AR signaling: Osteoblasts, osteocytes nd mesenchymal progenitors express AR. DHT binding can change osteoblastic differentiation and local RANKL or OPG balance (not important to know, but if you wanna know js tell me). But a good amt. of periosteal expansion requires proliferation of osteoprogenitors which is variant and..... BOOM, age dependent. So you're done by late teens. Like 17-18-19 means it's literally 99% over.

Estrogenic signaling: A lotta anabolic skeletal effects are attributed to androgens are actually mediated by aromatization to estradiol and then, ER signaling. Because DHT bypasses aromatase (as we read in 1.2.), it lacks a HUGGEEE PART that drives bone geometry in adults.

Cofactor/Chromatin context: Whether DHT changes a cell’s behavior depends on what helper proteins and DNA regions are available for the AR to work with. In mature bone (what we're talking abt), the genes that control growth and shape are mostly fucked, and only maintenance genes stay active. Even though DHT binds the AR it can’t turn on the old growth. So even a high affinity ligand like DHT yields constrained outputs.


4. Follicular Biology
Follicular Miniaturization: AAAANNNDDDD WE HAVE REACHED THE MAIN PART. Androgenic alopecia is a classic DHT mediated phenotype. In genetically susceptible follicles (AR polymorphisms, CAG repeat length, local SRD5A expression), DHT-AR transcriptional activity upregulates paracrine mediators like TGF-beta1/2, DKK1 that induce miniaturization, which, if your retard brain doesn't understand, basically means progressive shortening of the anagen phase, reduction of the hair follicle’s dermal papilla signals and replacement of terminal hair shafts with vellus hair.

Skin Texture: DHT actuvates sebaceous gland lipogenesis by AR driven expression of enzymes of lipid biosynthesis, increasing sebum production and pore prominence. Now obviously who on the fucking planet would want that? Yup, members of the pro DHT clan. JFL at them.

Regional specificity: The same androgenic milieu can masculinize secondary sexual traits (laryngeal hypertrophy, facial hair) but in a weird way cause hair loss on the scalp. This is a dichotomy. And this dichotomy is due to region specific AR cofactor expression and differential paracrine signaling in the ffollicular units (No need to get into details as our main topic has been cleared already)



SO, I GUESS THAT'S ENOUGH TO SHUT DOWN DHT COPES? BUT, I SERIOUSLY DON'T UNDERSTAND WHY ANYONE WOULD NEED DHT POST 17. REALLY MAKES ME CURIOUS.

​

mirin thread bro did read

 

[TheTD7]

mirin thread bro did read

thanks broski

 

[Chungusamongus]

mirin thread. Where did you gather all this info and endocrine knowledge? I’d like to dive deeper into this shit

 

[TheTD7]

mirin thread. Where did you gather all this info and endocrine knowledge? I’d like to dive deeper into this shit

Referred to medical books of my cousin and my dad + stuff i already learnt in studies, other books, research papers.

Just a whole lotta reading.

 

[Chungusamongus]

Referred to medical books of my cousin and my dad + stuff i already learnt in studies, other books, research papers.

Just a whole lotta reading.

any books you’d recommend as a base for newcomers?

 

[optimisticzoomer]

DHT sucks because it causes hair loss
But people who act like it’s useless are retarded. No one is developed at 16, and it is crucial for beard development. Some people look better with beards, or want to be able to grow one on occasion

Every other point against dht is complete cope. It does nothing to your skin

 

[Aryan Incel]

Good thread even ed is overstated this study shows that after 2 years ed on dut is very similar to that of a placebo group

How to Avoid Erectile Dysfunction with Dutasteride

Many men wonder how to avoid erectile dysfunction with dutasteride, an effective drug for treating alopecia and prostate hyperplasia. Although it can cause this side effect, […]

urologistandandrologistlondon.com

 

[TheTD7]

any books you’d recommend as a base for newcomers?

from what i have seen, it depends upon the person. i hated reading one book but understood everything from some other one. so it depends on you, you just gotta experiment.

 

[TheTD7]

It does nothing to your skin

Look, the functional unit is the pilosebaceous unit (hair follicle +sebaceous gland + infundibulum). The sebaceous gland consists mainly of sebocytes (lipid producing epithelial cells) that differentiate and holocrinely release sebum. Sebocytes express the AR and several steroid metabolizing enzymes

5AR isoenzymes (SRD5A1, SRD5A2) are differentially expressed in skin. SRD5A1 dominant in many skin sites and sebaceous glands while SRD5A2 is more abundant in some genital skin and some follicular compartments. This means local conversion of test to DHT occurs inside the very tissues that will respond to it

Skin is not a passive target. it’s a steroidogenic microenvironment. Circulating precursors (DHEA(S), androstenedione, test) enter the skin and are locally converted by enzymes (17 beta-HSD, 3 beta-HSD, and 5AR) to DHT in sebocytes and dermal papilla cells. So local DHT concentrations can be higher than serum and depend more on local enzyme expression and cofactor availability than on total serum T (which is why systemic testosterone levels alone don’t predict sebum/skin response perfectly, so we have that point clear too).

DHT binds AR with 5 x greater affinity and forms a longer lived AR-ligand complex compared with test. That gives DHT a larger transcriptional footprint per receptor occupancy in AR positive cells (including sebocytes) (Most of this i have already mentioned in the original post).

Liganded AR translocates to the nucleus, recruits coactivators and binds androgen response elements. In sebocytes AR activation increases transcription of genes for lipogenesis enzymes (fatty acid synthase, SCD, glycerol-3-phosphate acyltransferases), lipid droplet formation and cholesterol handling genes and differentiation markers that push sebocyte progenitors into a lipid filled secretory phenotype (holocrine differentiation). AR activity also synergizes with PPAR signaling pathways that further promote lipogenesis (or differentiation in simple termss). And the net result will be increased sebum production (volume) and altered sebum composition (changes in relative triglycerides, wax esters, free fatty acids, squalene) snd the composition shifts are important because certain free fatty acids and squalene oxidation products are pro inflammatory and comedogenic.

Androgens stimulate both sebocyte proliferation/differentiation (more sebum glands active) + enzymatic lipogenesis (more lipid output per cell). But the composition change is arguably more acne relevant than volume alone because it shifts the microenvironment toward conditions that favor Cutibacterium acnes activity and follicular inflammation

DHT can upregulate cytokines in sebocytes (IL-6, TNF-alpha in cell models) and modulate keratinocyte/sebocyte cross talk that promotes comedone formation and inflammatory lesions. I think its cleaar how mechanistic this is.

 

[MongolTurk]

The lack of libido after 6-9months of 5a-r inhibitors is brutal tho. Net benefit for baldingcels like me but still sucks

 

[optimisticzoomer]

The lack of libido after 6-9months of 5a-r inhibitors is brutal tho. Net benefit for baldingcels like me but still sucks

How is that brutal? Nuked libido is life
Sex and cooming is slavery

 

[TheTD7]

The lack of libido after 6-9months of 5a-r inhibitors is brutal tho. Net benefit for baldingcels like me but still sucks

@chadisbeingmade was on Dutasteride and experienced almost no side effects, if any.

 

[TheTD7]

JFL a pro DHT thread got posted a day after this.